A hazardous chemical is defined by the U.S. Occupational Safety and Health Administration as any chemical that has been scientifically shown to be a health hazard (causes acute or chronic health effects) or a physical hazard (combustible liquid, explosive, flammable, etc.). This federal agency estimates that there are 575,000 chemicals in the workplace, with 53,000 being potentially hazardous.¹ Considering that unplanned exposures and contamination can occur at any time during manufacturing, transport, storage, usage, or disposal of these chemicals, inevitably, emergency physicians can expect to occasionally be responsible for the management and care of a hazardous materials patient (see chapter 5, Disaster Preparedness).²

When managing a patient exposed to an industrial chemical, it is helpful to refer to the Material Safety Data Sheet and adhere to the recommendations regarding decontamination. Although the Material Safety Data Sheet will also include “first aid” recommendations (Table 204-1), the provider should also consult with a medical toxicologist or a regional poison control center to discuss case-specific hazards, optimal treatments, and dispositions. Contacting the regional poison control center facilitates data collection and analysis of toxicologic exposures. While many exposures produce immediate effects, some agents may result in delayed onset of symptoms that require at least 24 hours of observation (Table 204-2).

This chapter discusses common industrial toxins that produce primarily respiratory toxicity (Table 204-3) and those that cause metabolic toxicity. Toxic chemicals discussed elsewhere include nerve agents and vesicants (see chapter 8, Chemical Disasters); hydrocarbons (see chapter 199, Hydrocarbons and Volatile Substances); acids and alkalis (see chapter 200, Caustic Ingestions); organophosphates and carbamates (see chapter 201, Pesticides); metals (see chapter 203, Metals and Metalloids); oxidants (see chapter 207, Dyshemoglobinemias); and carbon monoxide (see chapter 222, Carbon Monoxide).

Several factors render children sensitive to chemical exposures.^3,4,5 Children have increased exposure to respiratory toxins because their minute volumes are higher, resulting in greater inhalational exposure. The smaller airway diameters and lesser ability to clear secretions render children more susceptible to inhaled toxins. Dermal absorption after exposure is also increased, because their skin is thinner and more permeable and they have a larger body surface-to-mass ratio. Children also are at risk for profound dehydration, resulting from vomiting and diarrhea secondary to toxic exposures. Many emergency protocols and antidote kits were developed for healthy adults, so dosing and care for pediatric exposures is usually scaled down from that used in adults.

A pregnant woman should be treated as any other adult patient because the best care for the fetus is proper care of the mother.⁶ Consult an obstetrician if there is a significant exposure or evidence of systemic toxicity.

Determinants of airborne agent toxicity primarily include factors such as concentration of the inhaled toxin, duration of exposure, and whether the exposure occurred in an enclosed space. Other influential factors include vapor density, allergic or nonallergic bronchospastic response, exertional state or metabolic rate of the victim, and unique host susceptibility such as underlying reactive airway disease, history of smoking, or extreme age. Aspiration of gastric contents may cause further pulmonary insult.

General management of the patient with toxic inhalation injury begins with removal from the source, supplemental oxygen for hypoxemia, and inhaled bronchodilators for bronchospasm. The physical examination should include inspection of the upper airway for evidence of singed nasal hair, soot in the oropharynx, facial or oropharyngeal burns, stridor, hoarseness, dysphagia, cough, carbonaceous sputum, tachypnea, retractions, accessory muscle use, wheezing, or cyanosis. Because of the potential for sudden deterioration in patients with upper airway injury, there should be a low threshold for endotracheal intubation. Irrigate the eyes and skin as appropriate.

Copious airway secretions, hypoxia, bronchospasm, and pulmonary edema should be anticipated. Prophylactic antibiotics and steroids are not routinely indicated following toxic gas inhalation. Steroids can be given if the patient has underlying reactive airway disease or toxin-induced bronchospasm, and prophylactic steroids and antibiotics can be considered after nitrogen dioxide exposure.⁷

Pertinent laboratory studies include arterial blood gas analysis with carboxyhemoglobin, methemoglobin, and lactate levels; whole-blood cyanide levels if persistent acidosis occurs (although this will not change immediate management); electrocardiogram monitoring; and chest radiography. The role for diagnostic or therapeutic bronchoscopy in inhaled toxin exposure is controversial.

Many highly toxic gases produced in large quantities in the industrial sector are potential agents for malicious use. Toxic gases of particular concern are those used in the battlefield or stockpiled—phosgene, chlorine, or ammonia. Additional toxicity can result from products of combustion such as hydrocarbons (see chapter 199, Hydrocarbons and Volatile Substances) or carbon monoxide (see chapter 222, Carbon Monoxide).

Phosgene was first used as a chemical agent of warfare in World War I, where it was responsible for 80% of all chemical gas fatalities. While stockpiled for potential use in World War II, it was never used in combat. Phosgene is no longer stockpiled by the U.S. military; however, it has widespread use in manufacturing and industry as a chemical precursor in the production of plastics, pharmaceuticals, dyes, polyurethane, and pesticides.^8,9 The heating of chlorinated fluorocarbons (Freon®) will also form phosgene gas and has caused poisonings in the refrigerator/air conditioner manufacturing and repairing industry.¹⁰

Phosgene release and contamination can be insidious. The gas is relatively water insoluble and therefore has poor warning properties. Only mild initial eye, nose, throat, and upper airway irritation are expected, and these may be entirely absent.⁸ Classically, when released, it forms a white cloud with a characteristic odor of newly mown hay. The major injury is an acid burn to lower airways as phosgene reaches the alveoli and hydrolyzes to carbon dioxide and hydrochloric acid.¹¹ Acylation of alveolar capillary membranes results in diffuse capillary leak and noncardiogenic pulmonary edema, which may be delayed for up to 24 hours.^11,12 Symptoms are typically dyspnea and chest tightness. If the exposure is massive, immediate dyspnea and mucous membrane and eye irritation may occur. The onset of dyspnea or pulmonary edema within 4 hours of exposure suggests a very poor prognosis.¹¹

Recovery usually occurs with respiratory supportive care and management of acute lung injury (noncardiogenic pulmonary edema).¹³ Do not provide supplemental oxygen until symptoms and signs of hypoxia develop or arterial oxygen saturation falls, and then administer at the lowest fraction of inspired oxygen to maintain arterial oxygen saturation above 94%.¹⁴ There is no benefit from IV and inhaled steroids or nebulized acetylcysteine.¹⁵ Nebulized β-agonists may reduce lung inflammation if given within 1 hour of exposure.^13,16 Exertion increases pulmonary edema from phosgene, so rest is mandatory.¹² If patients require intubation and mechanical ventilation for respiratory failure, a protective ventilation strategy with low tidal volume, low plateau pressures, and high positive end expiratory pressure should be used.^17,18 Observe and monitor even asymptomatic patients for 24 hours after acute exposure.

Chlorine is widely available in the industrial sector, in the setting of laboratories, paper manufacturing, swimming pool chemical distribution, and municipal water treatment.^19,20,21,22 Chlorine gas also has potential for use by terrorists.²³ When dispersed, this dense green-yellow gas has an acrid, pungent odor and, unlike phosgene, has excellent warning properties. Chlorine gas has intermediate water solubility, which is consistent with the observation that moderately exposed World War I soldiers exhibited both central airway damage and pulmonary edema.²⁴

Early inflammatory injury results from the formation of hydrochloric and hypochlorous acids and oxidants upon contact with moist membranes.²⁵ Immediate ocular and upper airway irritation along with nausea and vomiting are common following mild exposures.^19,26 More significant exposure results in coughing, hoarseness, and pulmonary edema, usually within 6 hours, with some exposures leading to acute respiratory distress syndrome.^20,27 Severe exposures may produce pulmonary infiltrates or edema visible on radiographs or CT scan.²⁸

Care is primarily supportive, with the use of humidified oxygen and bronchodilators as needed. Prophylactic antibiotics are not recommended. Nebulized sodium bicarbonate as a neutralizing therapy may improve pulmonary function during the initial 4 hours of treatment, but the long-term benefits are unproven.^21,29,30 Uncontrolled studies of both parenteral and inhaled steroids show improvement in airway resistance and arterial oxygenation but no improvement in the outcome with severe lung injury.⁷ Chlorine causes dermal injury at high concentration, and skin decontamination may be required. In patients with ocular symptoms, the cornea should be evaluated for a chemical burn. A moderately symptomatic patient should be observed for 24 hours, monitoring for delayed onset of respiratory complications.

Nitrogen dioxide and other nitrogen oxides are encountered in the form of silo gas (“silo filler disease”), as products of combustion, in industrial processes, or as components of military blast weapons, smokes, and obscurants.^31,32 These oxides have limited water solubility that results in primarily lower airway toxicity.³³ An exposure to a high concentration may only produce very mild initial discomfort. Slow conversion of nitrogen dioxide to nitric acid in the alveoli results in delayed alveolar injury and pulmonary edema.^31,34-36 A triphasic illness typically is seen with initial dyspnea and flulike symptoms, transient improvement, and then worsening dyspnea, which heralds the onset of pulmonary edema 12 hours after exposure.^32,34,36-38 Methemoglobinemia has been reported from nitrogen oxide exposure. Case reports describe benefit with early corticosteroid treatment for acute lung injury following nitrogen dioxide exposure,³⁸ although overall evidence is inconclusive.⁷

Ammonia is widely available; it is found in household and industrial chemicals and fertilizers and is used in the synthesis of plastics and explosives.³⁹ Ammonia is a highly water-soluble, colorless, alkaline, corrosive gas with a characteristic pungent odor that rapidly reacts with wet surfaces to form ammonium hydroxide. Ammonia has good warning properties due to its odor and immediate symptoms of mucous membrane, eye, and throat irritation. Lower airway involvement resulting in bronchospasm, pulmonary edema, residual reactive airway disease, and even permanent lung injury have been described following massive exposures, especially in those who are entrapped in enclosed spaces.⁴⁰

Treatment is supportive with humidified oxygen, bronchodilators, and anticholinergics.⁴¹ Concentrated ammonia, such as 8.4% ammonia hydroxide, is hazardous to the eyes, and symptomatic patients should undergo ocular irrigation followed by evaluation for corneal burns.

Cyanide has an infamous history. It was the agent used by Nazi Germany (Zyklon B) in the gas chambers during the Holocaust, by Jim Jones in the mass cult suicide at the People’s Temple in Guyana (commonly called “Jonestown”), for murder in over-the-counter drug-tampering incidents, and at the World Trade Center bombing in 1993.^42,43 Cyanide can be generated through natural and industrial processes (Table 204-4).

PATHOPHYSIOLOGY

Cyanide inhibits many metabolic processes, with its most toxic effect from binding with very high affinity to the ferric ion cytochrome a₃ portion of cytochrome oxidase within the mitochondria, resulting in an abrupt cessation of electron transport and oxidative phosphorylation, thus inhibiting cellular respiration.⁴³

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